In a way, dental decay is seen as an oral infectious disease which occurs as a result of adhesion and colonization of pathogenic bacteria to the tooth surface. Oral bacteria colonize the tooth surface according to the following mechanism. First, initial colonization bacteria such as Streptococcus oralis, Streptococcus sanguis, Streptococcus gordornii and Actinomyces naeslundii adsorb on the surface of enamel covered with a thin film (pellicle) of the saliva. Proliferation of these initial colonization bacteria comes along with their coaggregation, and then starts to form dental plaque. Once the dental plaque has matured, microflora undergoes its transition from facultative anaerobes to obligate anaerobes, and obligate anaerobes, typically such as Fusobacterium nucleatum, coaggregate with initial colonization bacteria. Subsequently, coaggregation of Fusobacterium nucleatum with periodontal pathogens such as Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia ensues, and eventually come to colonize on the tooth surface. Takemoto et al. suggested that Streptococcus mutans and Streptococcus sobrinus, which are bacteria related to dental decay, coaggregate with Fusobacterium nucleatum and therefore have a similar colonization mechanism (Non-patent Document 1).
Such coaggregation is caused by lectin•receptor interaction between bacteria, non-specific electrostatic interaction, adhesive action due to sticky polysaccharide synthesis, or non-specific hydrophobic interaction. The oral bacteria forming the plaque are different from the intestinal bacteria or skin indigenous bacteria and are composed of a flora which peculiarly resides in the oral cavity so that lectin•receptor interaction is thought to play a particularly important role in the colonization of the tooth surface by pathogenic bacteria. The “lectin•receptor interaction” is a stereospecific interaction between adhesin, which is a protein bound to the surface layer of bacteria, and a receptor structure on the surface layer of another bacteria. Most of the lectin•receptor interaction develops hydrocarbon-specific binding.
A lactose sensitive adhesin is a common lectin present in the plaque forming bacteria and it specifically recognizes β-galactoside in lactose. Lactose sensitive adhesin is present widely in the oral bacteria and it is involved in the coaggregation of the genera Actinomyces, Streptococcus, Porphyromonas, Prevotella, Fusobacterium, Haemophilus, Capnocytophaga, Veillonella, Neisseria and Selenomonas (Non-patent Document 2).
Inhibition of the tooth surface from the colonization by pathogenic bacteria is thought to be effective as preventive means of oral infectious diseases. There are, for example, reports on the use of galactose or lactose to prevent adhesion of plaque to teeth (Patent Document 1) and use of a fatty acid sugar ester in which at least one antibacterial fatty acid having from 10 to 16 carbon atoms has formed an ester linkage with fructose or galactose (Patent Document 2).    [Patent Document 1] JP-B-S58-11924    [Patent Document 2] JP-A-2000-159675    [Non-patent Document 1] Journal of Periodontal Research, Vol. 30, p 252-257    [Non-patent Document 2] Infection and Immunity, Vol. 57, p 3194-3203